Intraocular kainic acid injection suppresses fast axonal transport in the developing rat optic nerve.

A single intraocular injection of 1 or 3 nmol kainic acid (KA) into the right eye of rats aged 5 days postnatal (5 dpn) significantly reduced the incorporation of 3H-proline into retinal proteins and suppressed the amount of 3H-proline-labeled materials fast axonally transported in the optic nerve for at least 2 weeks thereafter. Intraocular KA injection within this dose range had no adverse effect on the optic axon population compared to normal nerves determined at 21 dpn; however, doses above 3 nmol (i.e., 6 nmol) caused significant axonal degeneration. Although partially recovered by 21 dpn this effect of KA on protein synthesis and axonal transport suggests that, as in the adult, retinal ganglion cells are also KA-sensitive during postnatal development.